Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
355 Cards in this Set
- Front
- Back
|
Largest family of viruses
|
Picorna virus
|
|
|
Best known and studied Picorna virus
|
Polio virus
|
|
|
Picorna virus is ____ so it does not cause ______ problems
|
naked, enteric problems
|
|
|
# of picorna viruses, divided into _ genera
|
230, 9
|
|
|
2 genera of picorna viruses
|
enterovirus and rhinovirus
|
|
|
Structure of Picorna
6 |
+ RNA
icosahedryl form naked 12 pentomers 5 units of protein 4 structural polypeptides |
|
|
genome of picorna resembles
|
mRNA with 5' end VPG
|
|
|
picorna virus is _____ to host based on tightly regulated ________
|
specific
cell receptors for tropism |
|
|
VP1 binds to receptor at ________
|
canyon
|
|
|
Antivirals are looking into modifying ____________
|
canyon
|
|
|
VP4 is released and causes
|
virual structure to weaken and form channel into host
binds directly with ribosome RNA pol makes template = new genome |
|
|
time it takes to make polyproteins (picorna)
|
10-15 min
|
|
|
capsid is formed from __ & ___ in picorna
|
VP2 and VP4
|
|
|
replication cycle takes _______ for picorna
|
3-4 hours
|
|
|
Enterovirus enters
|
though oropharynx and foes to respiratory or gut
|
|
|
in gut enterovirus
|
replicates in mucosal cells-- no infection
|
|
|
in respiratory enterovirus attacks
|
mucosal and lymph tissue
causing primary viremia ( reticulo endo, spleen and liver) 2nd viremia due to tissue damage |
|
|
enterovirus is shed in
|
resp and gut, easy to get in crowded and unsanitary conditions
|
|
|
echo stands for
|
enteric cytopathic human orphan
|
|
|
3 enteroviruses
|
echo, polio, coxsackie
|
|
|
difference between coxsackie A and B
|
a- more severe in adults
b- more severe in babies |
|
|
6 factors affecting severity of viruses
|
viral serotype, infecting dose, tissue tropism, portal of entry, age- gender- health, pregnancy
|
|
|
incubation period of enteroviruses
|
1-35 days (respiratory infection is shortest)
|
|
|
Polio virus commonality
infects the ____ --> ____ |
rare in US because of vaccines
skeletal muscle --> brain |
|
|
polio virus targets ______ meaning____ and the _____ of the _____ leading to ____
|
cytolytic neurons, motor neurons
anterior horn of the brain stem leading to paralysis |
|
|
4 types of polio virus
|
assymptomatic
polio myelitis minor aseptic meningitis paralytic poliomyelitis major |
|
|
% assymptomatic polio
|
90%
oropharyngeal and gut only |
|
|
% polio myelitis minor
aka _________ causes |
5%
abortive poliomyelitis febrile |
|
|
aseptic meningitis %
aka affects |
1-2%
non paralytic polio meningitis affects CNS, meninges |
|
|
Paralytic poliomyelitis Major %
|
2 % most severe
1st --> minor form then subsides travels to brain and gets severe flaccid paralysis |
|
|
flaccid paralysis
|
can't move but can still sense things
|
|
|
cause of paralytic poliomyelitis
|
85% ause by PV-1
|
|
|
recovery of polio (3 types)
|
hard to predict
complete (1 mo- 2 years) residual paralysis or death |
|
|
most severe of most severe (polio)
affects % mortality hospitals cure for this |
type 4-- Bulbor polio myelitis
pharynx, vocal cords, respiratory 75% mortality iron lungs |
|
|
30 years after children infected with polio can get
|
post polio syndrome
neuron degradation increased and have same symptoms |
|
|
% of people showing post polio syndrome
|
20-80%
|
|
|
Coxsackie and echo are both
|
assymptomatic or mild
|
|
|
coxsackie A can cause (5)
and is |
herpangina (herpes like lesions) around soft pallet and uvula, sore throat, fever, vomiting
self limiting |
|
|
Coxsackie A16
|
hand foot and mouth disease
-- lesions on those areas |
|
|
coxsackie B important to ___ because
also called (3) causes |
more important in neonates (heart failure)
pleurodynia, bornholm disease, devil's grip fever and chest pain, recurring. in pancreas---> islet destruction--> insulin dependent diabetes |
|
|
Echo causes
similar ___ in ____ |
fever, rash (petichial), cold like sx.
similar rash in Neisseria meningitis |
|
|
Dx of echo
|
CSF (if meningitis)
look at lymphocytes, glucose norm to slightly low, protein norm--> slightly high |
|
|
tissue culture of coxsackie A
|
grown in mice, RT PCR and immunoassays
|
|
|
treatment and control of enterovirus
|
inhibit penetration (piecornaril)
vaccines (against polio) |
|
|
2 types of polio vaccines
|
SALK- inactive polio virus
Sabine- attenuated oral polio virus (immunized by proxy) |
|
|
difference between salk and sabine
|
salk- IPV- inactive
sabine- OPV- attenuated, shed by people and others can get attenuated version---> community immunization |
|
|
Rhinovirus has ____ serotypes and can not live in the ____ tract.
infection spread via likes temp |
100
GI aerosols and hands... enters mouth nose and eyes 33 degrees |
|
|
Rhinovirus infected cells dump
|
bradykines and histamine
|
|
|
Unique thing about rhino virus
|
only 1 virion needed to infect
|
|
|
% of resp infections are rhinovirus
|
50%
|
|
|
Corona virus means
causes bad in___ because prevelancy |
crown or halo, looks like solar corona
causes cold sx and gi events (babies) can cause necrotizing enderocolitis most prevalent after rhino virus |
|
|
Well known corona virus
|
SARS
|
|
|
Corona virus structure
|
envelope
longest genome of RNA virus club shaped surface projections - can survive in GI |
|
|
infection of coronavirus
|
oral fecally, inhalation
|
|
|
4 glyoproteins of coronavirus
|
E1- transmembrane, matrix
E2- attachment, membrane fusion of env. to host N- nucleoprotein of core E3- hemagglutinin neuramidase |
|
|
corona virus increase sx in people with
|
prexisting resp. problem
worry about pneumonia |
|
|
SARS is a _____ pneumonia
mortaility % causes |
atypical
10% high fever, chills, headache, dizzyness, malaise, myalgia, cough Breathing problems |
|
|
location of infection of SARS
|
china- hong kong- vietnam- canada
|
|
|
dx of SARS
|
BSL 3, RT PCR, EM of stool
|
|
|
treatment of mumps
|
quarantine
|
|
|
Calcivirus is typically ____ or _____ shaped
main one we talked about |
cup or 6 pointed star shaped
Norovirus |
|
|
norovirus resembles
structure (4) difference between other calciviruses |
picorna virus
+ RNA with VPG, naked, round pleuomorphic virus can not grow in cell cultures |
|
|
Norwalk like proteins bind to____
early proteins are late proteins are |
A,B,H Ag on RBC
RNA poly and enzymes structural |
|
|
Norovirus causes
|
gastroenteritis-- no RBC problems
|
|
|
incubation period of norovirus
resolves in how long shedding virus |
24-48 hours
resolves in 12-60 hrs 2 weeks after sx, still shedding virus |
|
|
norovirus attaches to
causes |
intestinal brush borders
causing watery diarrhea and vomiting |
|
|
Norovirus commonly found on
% of food borne gastroenteritis cause by this |
cruise ships
50% |
|
|
Dx of norovirus
treatment |
PCR of stool or vomit
clean hands, clean h20, wash dishes treat sx. give h20 and electrolytes |
|
|
family that makes syncytia
|
paramyxoviridae
|
|
|
3 groups of paramyxoviridae and their key diseases
|
morbillivirus- measles/ rubella
paramyxovirus- mumps pneumovirus- RSV |
|
|
RSV
|
respiratory syncytial virus- fatal in infants
|
|
|
zoonotic paramyxoviruses
|
nipah and hendra
cause encephalitis |
|
|
vaccine for measles
|
MMRVZ
only one serotype rarely hear of measles or mumps now |
|
|
paramyxo structure
|
- RNA, helical nucleocapsid mad of Nucleoprotein, polymerase phosphoprotein, and large protein
pleomorphic envelope with Matrix protein |
|
|
2 glycoproteins of paramyxo virus
|
F (fusion) protein
VAP made of Hemagglutinin neuramidase hemagglutinin and G protein |
|
|
rubiola attaches to activated ______ on CD __ and ___
|
T and B cells
CD46 and CD150 |
|
|
replication of paramyxo virus
|
RSV into cell cytoplasm: transcription, protein synth, genome repl, mRNA and + RNA template, individual proteins
|
|
|
measles- rubiola
% acquired by age 20 sx. |
90%
rash, high fever, cough, conjunctivitis, coryza |
|
|
% reduction since vaccine (measles)
|
99.5%
|
|
|
infection of measles
contagious with |
cell-cell usually with lysis
persistent in brain highly contageous with resp. droplets |
|
|
replication of measles occurs in
incubation period sx caused by |
upper resp. tract and spreads via T and B cells
incubation of 7-13 days release of cytokines |
|
|
Sx of measles
|
prodrome--> fever, CCC &P
2 days later koplik spots 12-24 hours later measles rash spreads macropapular (1-2 days0 fades in the order it came lifelong immunity |
|
|
CCC&P
|
cought conjunctivitis, coryza and photophobia
|
|
|
koplik spots
|
blisters in mouth
"grains of salt surrounded by red halo |
|
|
dangerous age for measles
|
1-5 (60% die from pneumonia and 2nd infections)
|
|
|
% of catching measles with out vaccine
|
85%
95% symptomatic |
|
|
% of deaths from measles encephalitis
|
15%
|
|
|
SSPE
|
subacute sclerosing pan encephalitis
change in personality, memory and behavior jerking--> blindness |
|
|
Dx of measles
|
by sx.
tissue culture impossibly, unless before rash CPE- giant multinucleate cells RT-PCR and ELISA (seroconversion) |
|
|
treatment and prevention
|
VACCINE
no anti-viral treatments treat sx. |
|
|
Parainfluenza causes
|
cold like sx--> severe resp. tract inf.
|
|
|
# of serotypes in parainflu
each one causes |
4
1-3 cause croup 4 is mildest |
|
|
croup
|
laryngotrachieobronchitis
bad cough |
|
|
cells infected by parainflu
|
upper resp tract epithelial cells
cause syncytia and lysis |
|
|
partial immunity of parainflu
|
reinfection is common
|
|
|
parainflu found mainly in
|
kids under 5
problem in pediatric ward pass through resp. droplets |
|
|
clinical sx. of parainflu
|
croup, swelling, inflam, cough, closes airway "seals bark" 48 hours--> better
|
|
|
treatment and control
|
treat symptoms
use cold nebulizers and clean air |
|
|
Virus that causes Seal's bark
|
Parainfluenza
|
|
|
mumps is closely related to
|
parainflu II, but no cross immunity
|
|
|
mumps causes a
|
benign viral parotitis
|
|
|
mumps is rare because of
|
MMR vaccine
|
|
|
# of serotypes of mumps
|
1
|
|
|
mumps tranmitted via
|
resp droplets, person to person
|
|
|
sx. of mumps
|
7 days, none. but most infectious
replication and shedding in epith. cells of resp tract--> parotid gland swelling of 1orboth parotid glands, fever many are assymptomatic |
|
|
mumps is serious in
|
adults. can spread to testes causing inflam and sterility, ovaries, pancreas, thyroid, viremia--> up to 50% CNS involv.
|
|
|
how many days post sx. do people shed mumps
|
5 days
up to 2 weeks in urine (non contagious) |
|
|
dx. and treatment
|
multinucleate cells
serological testing no antivirals-- vaccines |
|
|
RSV
difference between other paramyxo viruses |
respiratory syncytial virus
of the pneumovirus genus no Hemagglutinin or neuramidase |
|
|
RSV is known for being
|
the most common fatal acute resp. tract infection (infants and children)
important in nurseries and hosp (NICU) |
|
|
Prevelance of RSV in children
|
most have it by age 2
can get reinfected |
|
|
process of rsv infection
|
viral invasion of epithelial cells --> syncytia, necrosis of bronchi and bronchioles
necrosis caused by mucus plugs with fibrin and necrotic material airway obstruction |
|
|
RSV spread by
|
resp secretions and fomites
|
|
|
incubation of RSV
|
4-5 days
initial cold sx--> pneumonia if goes to lower resp.(25-33%) ~1% hospitalized |
|
|
Sx. of RSV
|
wheezing
|
|
|
Dx of RSV
|
cell culture is hard, PCR but neg doesn't mean neg
|
|
|
treatment of RSV
|
supportive, nebulizer, humidifier, passive immunity
no vaccine |
|
|
Human metapneumovirus
|
similar to RSV, differentiate by PCR
connection to ear infections treat sx. |
|
|
Nipah '98 and Hendra '94
|
zoonotic--> humans
high mortality fruit bats of asia. |
|
|
7 types of paramyxoviruses we covered
|
measles
mumps parainfluenza RSV human metapneumovirus Nipah Hendra |
|
|
types of orthomyxovirus that affect humans
|
influenza A and B
|
|
|
structure of influenza
|
- RNA segmented, enveloped, pleomorphic
|
|
|
Envelope of influenza made of
|
HA and NA
|
|
|
what causes new strains of influ
|
segmented RNA reassortment and mutations
|
|
|
membrane proteins
|
M2- causes channel, allows uncoating
|
|
|
M1 protein
|
matrix- assembly protein
|
|
|
how many segments of A and B influ
|
8, helical nucleocapsid segments
each has - sense RNA associated with NP and transcriptase |
|
|
Difference between A,B, and C influ
|
A & B are human
C is non human C only has 7 segments, A and B have 8 only influ A has mutation in HA protein causing pan and epidemics |
|
|
HA is a
3 fns. |
spiked trimer, cleaved by proteases
used in viral attachment, binding to sialic acid, and fusion to cell membrane |
|
|
NA is a
|
tetramer with enzyme activity
cleave sialic acid and prevents cell clumping target for antivirals |
|
|
7 steps of orthomyxovirus replication
|
1- bind
2- uncoating 3- transcription 4- translation of M&N in cytoplasm, M2 insertion into membrane HA and NA go to cell surface 5- replication in nucleus 6- assembly 7 release (8 hours post infection) |
|
|
during binding of orthomyxo what happens
|
HA: sialix acid--> internalized and transported via a vesicle to endosome --> acidified and bends exposing hydrophobic fusion promoting regions--> binds to envelope
|
|
|
Uncoating in orthomyxo causes
|
nucleocapsid release into cytoplasm --> nucelus
|
|
|
during transcription of orthomyxo what is stolen from host
|
methylated cap of host RNA to bind to ribosome
|
|
|
orthomyxo causes_________ by
|
upper resp. infection
kills mucus secreting cells and cilliated epithelial cells, no defense so prone to 2nd infections |
|
|
orthomyxo serious if it
|
hits lower resp tract infection
cells damaged, long time to repair |
|
|
phases of orthomyxo sx.
|
febrile phase- due to interferon and cytokine involvement
flu sx- fever malaise, headache, myalgia-- form Ab to specific strains |
|
|
4 ways to name flus
|
type (ABC)
original isolation date of isolation antigenic types (not flu B) |
|
|
annual epidemics of influ caused by
|
drifts, mutation in HA and NA genome- local outbreaks
|
|
|
Pandemics are due to
|
shifts or reassortment (only Flu A)
|
|
|
Shifts and reassortments happen in
|
pigs and birds, coinfection in one then hybrid strains are transferred to humans
|
|
|
1918
|
Spanish influ- WWI
killed 20-40 million |
|
|
1977
|
Bird flu
chickens in china--> spread H5N1 virus- not reassortment, but very virulent only control--kill birds did not travel person to person |
|
|
severity of influ
|
dependent on age, health, immune, preg.
|
|
|
Sx. of influ
|
prodrome- few hours
abrupt fever, chills, myalgia, weakness, fatigue, loss of appetite, non-productive cough 7-10 days recovery unless complications |
|
|
dx. of influ
|
ag to hemagglutinin
PCR quick kit |
|
|
treatment of influ
|
treat sx.
some antivirals may be available control by immunization |
|
|
immunizations to influ
|
extracts of HA and NA (3 strands mixd)
|
|
|
Rhabdovirus
|
Rod virus
natural pathogen to animals and plants (Not human) |
|
|
2 types of rhabdovirus
|
VSV- vesiculostomatitis virus
lysavirus- rabies and other rabies-like virus |
|
|
rhabdo virus structure
|
simple- bullet/ rod shape
spiked envelope 5 proteins (G, N, NS, L,M) enveloped helical nucleocapsids - ss RNA |
|
|
unique feature of rhabdo nucleocapsid
|
looks like striations because it is coiled
|
|
|
Rabies replication
|
G protein binds to host receptor and affects CNS
internalized via endocytosis, fuses with cell membrane and uncoats-- > cytoplasm. gene transcribed --> 5mRNA --> 5 proteins & full lenght--> reassembly (seperate from envelope)--> enveope surrounds genome |
|
|
what causes coiled shape of rhabdo virus
|
genome combines with N,L,NS proteins then with matrix protein during reassembly
|
|
|
difference between rhabdoviruses and rabies
|
rabies does not lyse cell, other rhabdo viruses do
|
|
|
rabies is a
transmission through (3) |
classic zoonotic infection
bites, aerosols (bat caves), tissue transplants |
|
|
incubation period of rabies
|
long--> several months
|
|
|
process of infection in rabies
|
infects original site--> locolaized--> retrograde axonic transport--> infects neurons at AchR or ganglioside receptors--> iinfects dorsal root ganglia
|
|
|
rabies causes
and affects (4) places |
encephalitis, neuron degeneration
skin of head and neck, salivary glands, retina, cornea |
|
|
treatment
|
block antibody spread to neurons
killed rabies vaccine--> immune system reacts |
|
|
urban vectors of rabies
sylvanic |
Dog (#1 worldwide) Cats (US)
raccoons and bats |
|
|
first Sx of rabies
|
prodrome (2-10 days)
fever, malaise, headache, pain/itching at bite site, GI fatigue, anorexia |
|
|
2nd sx. of rabies
|
neurological at 2-10 days--> sever neurological
hydrophobia, seizures, disorientation hallucination paralysis--> coma --> death |
|
|
post exposure prophylaxis to rabies
|
treat wound
vaccine--> immune response 5 vaccines over 1 months (day 1, 3, 7, 14,28) intermuscular |
|
|
2 types of rabies vaccines
|
HDV- human diploid cell vaccine
HRIG- human rabies IG |
|
|
dx. of rabies
|
look at brain neurons of rabid animal
look at negri bodies in neurons of brain |
|
|
Filovirus- 2 types
|
Marburg and ebola
|
|
|
structure of filoviruses
|
filamentous, enveloped, - ss RNA with 7 proteins, helical nucleocapsid
|
|
|
filovirus is considered
and causes found mainly in |
severe--> fatal
hemorrhagic fever Africa |
|
|
Replication of filovirus
|
replicate in monocytes, macr, dendritic cells causing necrosis of liver spleen lymph and lungs
or in endo of blood vessels --> hemorrhagic --> hypovolemic shock --> edema glycoprotein (Ebola) |
|
|
Marburg
|
found in germany
caused by HEALTHY african green monkeys |
|
|
Ebola
|
named after a river in Zaire, congo
spread via animal and blood/ body secretions |
|
|
sx. of ebola
|
headache, malaise, myalgia, nausea, vom, diarrhea, rash, hemorrhaging (GI tract)
|
|
|
% fatality in Ebola
|
90
|
|
|
Dx of ebola
|
level 4 iso lab
RT PCR look for eosinophilic cytoplasmic inclusions |
|
|
treatment of ebola
|
infected people quarantines
infected animals sacrificed |
|
|
Borna virus
|
relatively new
found in horses in germany association with schizophrenia |
|
|
structure of bornavirus
|
- RNA
enveloped 5 proteins (L, N, P,M,G) |
|
|
proteins of bornavirus
|
L- polymerase
N- nucleoprotein P- phosphoprotein M- matrix protein G- glyco and envelope |
|
|
replication of borna virus
|
nucleus, similar to orthomyxovirus--- NOT SEGMENTED
|
|
|
Disease of bornavirus
|
neurotropic, attacks nerves and travels through parenchymal cells of organs
t cells keep in check, but tissue damage --> brain problems |
|
|
Dx of borna virus
|
blood mononuclear cells (Rt PCR)
|
|
|
animals infected with borna virus sx.
|
learning and memory loss--> fatal meningioencephalitis
resembles: schizophrenia, bipolar, depression, autism |
|
|
treatment of bornavirus
|
antiviral- ribavirin
|
|
|
Reovirus means
4 types |
Respiratory enteric orphan
orthoreo virus, rotavirus, orbvirus, coltivirus |
|
|
orthoreovirus
|
mammalian reo virus--- mostly assymptom
|
|
|
orbivirus and coltivirus
|
arbovirus-- tick transfer
|
|
|
rotavirus means
important in |
wheel
infants-- infantile gastroenteritis |
|
|
structure of Reovirus
|
icosahedral ds RNA with a double layered capsid
outer capsid is structural 10 segmented RNA |
|
|
virus called "double double"
|
Reo virus
|
|
|
# of segments in rotavirus
|
11
|
|
|
Rotavirus has 2 glycoproteins outside of capsid
|
VP1, NSP4 (nonstructural protein)
|
|
|
assembly of rotavirus
|
make envelope--> take glycoprotein --> lose envelope
|
|
|
core of rota virus involved in
|
hemagglutination, viral attachment, Ab neutralization
|
|
|
rotavirus transmitted by
|
oral transfer
|
|
|
Rotavirus dx. via
|
aggregation of proteins and + RNA into inclusion bodies in the cytoplasm
|
|
|
Reo vs. Rota
|
reo--> capsid proteins and core shed via lysis
rota--> core associated with ER proteins and buds in, takes pseudoenvelope, loses envelope and released via lysis |
|
|
Orthoreovirus
|
mammalian
ubiquitous (sewage and water) |
|
|
process of orthoreovirus
|
ingestion--> ISVP--> mcells of small int --> lymph--> replicate --. viremia
|
|
|
sx. of orthoreovirus
|
assymp --> cold
|
|
|
what causes world-wide infantile diarrhea
|
rota- enterics
|
|
|
rota-enterics enhanced by
|
trypsin
|
|
|
serotype of rota-enterics based on
|
VP7 and VP4
|
|
|
amount of orthoreovirus shed in stool
|
10^10 particles/ gram of stool
|
|
|
orthoreovirus protein that affects h20 reabsorption
|
NSV4
|
|
|
rotavirus is dangerous to
|
children in underdeveloped countries
|
|
|
most common cause of serious diarrhea in children is
|
rota virus
|
|
|
rota virus transmitted via
|
oral-fecal contract and fomites
|
|
|
clinical sx. of rota virus
|
48 hour incubation, gastroenteritis,vom, diarrhea, fever, dehydration
self limiting, but need to treat sx. |
|
|
dx. of rota virus
|
EM (old)
quick kits vaccine in US |
|
|
Coltivirus means
vector |
CO tick fever
wood tick |
|
|
coltivirus infects
|
RBC precursors--> mature RBS contains virus (non detectable) --> endothelial damage --> hemorrhage or meningitis/ encephalitis
|
|
|
sx. of coltivirus
|
3-5 day incubation
prodrome--> attacks organs and maculopappular or petechial rash KEY: Leukopenia |
|
|
specific organs attacked by coltivirus
|
conjunctivitis, lymphadenopathy, hepatosplenomegaly
|
|
|
what disease must coltivirus be differentiated from
|
rocky mountain spotted fever (Rickettsia)
|
|
|
amount of time before donating blood after coltivirus
|
forever... can not donate again
|
|
|
prevention of coltivirus
|
avoid bites, wear clothing and repellants
can get virus from first bite |
|
|
Togavirus means
3 main groups |
latin for cloak
alpha (arbo), rubi (rubella), arteri (non human) |
|
|
toga virus is similar to
|
flavi virus
|
|
|
alphavirus structure
|
icosahedryl
+ ss RNA enveloped spiked appearance lumpy capsid |
|
|
replication of alphavirus
|
endocytosis,fusion with membrane, enter cytoplasm, attach to ribosome--> poly protein, 2/3= NSP1-4, 1/3 structural, reassembly and release
|
|
|
alphavirus causes
4 |
assymp--> encephalitis
EEEV WEEV VEEV chikungynya |
|
|
EEEV
WEEV VEEV chikungnya |
eastern equine encephalitis virus
western " " venezyelan "" to bend up (swahili) |
|
|
flavivirus structure
|
similar to alpha
+ss RNA icosahedral envelope smaller |
|
|
what enhances flavivirus infectivity and by how much
|
attachment to Fc receptors when coated with antibody
200-1000x |
|
|
2 difference between flavi and alpha virus
|
1) structural proteins made first, then enzymatic-- lag time before sx. appear and slows down replication
2) envelope comes from intracellular vesicles not cell membrane |
|
|
flavivirus causes
|
benign--> aseptic meningitis, encephalitis, hemorrhagic disease
|
|
|
5 encephalitic disease of flavivirus
2 hemorrhagic |
west nile, st. louis fever, japanese fever, murray valley fever, russian spring-summer virus
dengue fever, yellow fever |
|
|
dengue fever
|
break bone fever
Northern S.A. shock syndrome |
|
|
shock syndrome
|
severe shock and internal bellding
from vaccine |
|
|
yellow fever
|
jaundice because of liver, heart, kidney failure
massive GI bleed and black vomit 50% mortality |
|
|
arbovirus natural vectors
terminal host |
birds, monkeys, rodents
horse or human |
|
|
what flavivirus can be spread human to human
|
west nile
|
|
|
immune response to flavivirus
|
interferon stimulated
inflammation--> tissue destruction --> CNS involvement hemorrhage--> activation of complement |
|
|
cycle of flavivirus
|
slyvatic form (monkeys)
urban form (man) |
|
|
dx of flavivirus
|
CPE, RTPCR, immunofluorescence
|
|
|
treatment of flavivirus
|
treat sx. control vector
|
|
|
Walter Reed
|
1930
yellow fever spread via aeded aegupti vector control |
|
|
vaccines against yellow fever and dangue fever
|
yellow fever-- for travellers
dangue fever-- none, causes shock syndrome |
|
|
Rubells means, called, part of family
|
little red, german measles, togavirus
|
|
|
unique thing about rubella compared to other togaviruses
|
not spread via arthropod
spread via respiratory |
|
|
diseases from rubella
|
congenital cataracts, severe congenital problems, mental retardation, birth defects (teratogenic)
|
|
|
host for rubella
|
only human
|
|
|
disease process of rubella
|
upper resp--> 14-21 day incubation--> prodrome (2 weeks) assymp--> lymph nodes --. viremia
|
|
|
key symptom of rubella
|
lymphadenopathy
|
|
|
still infections ____ after rash in rubella
|
2 weeks
|
|
|
rubella acts on fetus by
|
causing chromosomal structure damage
|
|
|
highest risk for babies is up to age
|
20 weeks
|
|
|
Bunyaviridae and Arenaviridae
|
- RNA
enveloped zoonotic cause encephalitis and hemorrhagic diseases |
|
|
bunya virus transmitted via
called a |
mosquito, tick, flies
"super group" 200+ viruses |
|
|
4 subgroups of bunya virus
|
bunyavirus
phlebovirus nairovirus hantavirus |
|
|
hantavirus is unique because
|
vector is rodent not arthropods
|
|
|
bunyavirus has 3 unique strands of RNA that can
|
form circles in lacrosse virus and california encephalitis virus
|
|
|
proteins in bunya virus
|
L- polymerase
m- non-structureal s- NSs and NSm NO matrix proteins! |
|
|
diseases of bunya virus are similar to
|
togaviruses
|
|
|
bunya virus causes
|
damage to nerves, cerebral edema, encephalitis, hepatic necrosis, rift valley fever, hemorrhagic (hanta and crimean congo hemorrhagic fever)
|
|
|
2 hemorrhagic fevers caused by bunyavirus
|
hanta and crimean congo hemorrhagic fever
|
|
|
arenaviridae is transmitted via
|
rodents
|
|
|
California encephalitis group virus
found in |
north america
|
|
|
hanta virus outbreak in 1993
|
in four corners
traced to deer mouse population called sin nombre |
|
|
hanta virus is a
sx. |
non specific febrile disease
48 hour incubation --> fever 3 days encephalitis--> 2nd sx. |
|
|
2nd sx of hanta virus
|
fever headache lethargy vom
50% have seizures (meningitis) last 10-14 days |
|
|
% mortality
|
1
|
|
|
hemorrhagic sx. of hanta virus
|
rift valley fever (petechia)
bloody nose, vom gums and stool lead to blood pneumonia mortality 50% |
|
|
hantavirus--> lungs
|
fever, aches, pulmonary edema, resp. failure --> death (w/in days)
|
|
|
Dx of hantavirus and treatment
|
RT PCR, serological confirm
none treat sx. avoid vector contact, control vector |
|
|
Arenavirus
causes |
sandy
LCM and 3 hemorrhagic fevers |
|
|
LCM
|
lymphocytic choriomeningitis
|
|
|
3 hemorrhagic fevers caused by arenavirus
|
Lassa, Junin, Machupo
|
|
|
structure of arenavirus
|
pleomorphic, enveloped, ribosomes on virion
2 ss circular RNA |
|
|
2 major proteins of arenavirus
|
L- transcription
s- nucleoprotein/ glycoprotein |
|
|
replication of arenavirus ocurs in
|
cytoplasm
|
|
|
arenavirus found in
transfered via |
Africa and SA
rodents, saliva urine feces, contact with dried virus |
|
|
LCM vector
Lassa vector |
hamster/ house mouse
african rodent and human-human via secretions |
|
|
white water arroyo arenavirus
|
1999-2000 new virus
infect t cells= tissue destruction after 10-14 day incubation |
|
|
sx. of arenavirus
% mortality |
hemorrhagic fever--> coagulopathy, petichiae, visceral hemorrhage
50% mortality |
|
|
Dx of arenavirus
treatment |
RT PCR- need L3 or L4
lassa fever- treat with ribavirin |
|
|
The ultimate parasite
|
retrovirus
most studied of all groups |
|
|
structure of retrovirus
|
envelope
+RNA |
|
|
Retrovirus replication
|
RNA dependant DNA pol
DNA intermediate cDNA then transcribed with host chromosome |
|
|
% of chromosome retroviruses become
|
1
|
|
|
3 subfamilies of retroviruses
|
oncovirinae
lenticirinae spumavirinae |
|
|
oncovirinae- unique
causes |
only retro that can transform/ immortalize
HTLV |
|
|
Lentivirinae
causes |
slow virus--> neurological problems and immunosuppression
HIV--> AIDS HIV-2 varient in W. Africa |
|
|
Spuma virinae
|
foamy virus- CPE
non human |
|
|
classification of retroviruses based on
|
disease, hosts, tissue tropism, morphology, genetic complexity
|
|
|
structure of retrovirus
|
spherical RNA
envelope (from host plasma mem) capsid 10-50 rtases spike form timers fro binding |
|
|
genome of retroviruses
|
resembles mRNA
3 major genes (GAG, POL, ENV) |
|
|
GAG
|
gene for goup specific antigens, capsid matrix and NA binding proteins
|
|
|
end of genome has
|
LTRs
oncogenic--> oncogene found here |
|
|
places HIV can bind to cells
|
CD4 protein AND
CCR5 (macrophages) or CXCR4(t cell cytokines) |
|
|
antivirals are looking into
|
inhbiting CD4 binding with HIV
inhibiting reverse transcriptase from working with virus |
|
|
binding with CD4 and CCR5 or CXCR4 cause
|
conformational change with GP120 bringing virus to membrane with GP41
|
|
|
early replication of HIV
|
need reverse transcriptase
makes - cDNA attaches LTR at either end, dscDNA spliced into host chromosome with integrase |
|
|
startes late replication of HIV
|
splicing
|
|
|
viral DNA is a ____ once spliced
|
provirus
|
|
|
jobs of host cell for HIV
|
active cell replication and recognition of LTR
needs to beable to transcribe genome |
|
|
2 phase transcription found in
steps are |
complex retroviruses
transcribes Tax and Rex double splicing mechanism |
|
|
tax vs. rex
|
tax- transcriptional activator
rex- structural protein early- more tax, less rex late less tax, more rex |
|
|
6 accessory proteins of HIV
|
TAT
REV NEF VIF VPU VPR |
|
|
TAT
REV |
transcriptional activator
regulates and promotes viral mRNA |
|
|
NEF
|
imperative for HIV--> AIDS
reduces CD4 and mHC receptors, alters signalling, reculated cytotoxicity, maintains viral loads |
|
|
VIF
|
promotes assembly & maturation
binds antiviral proteins |
|
|
VPU
|
reduces CD4 expression and enhances viral release
|
|
|
VPR or VPX
|
VPR (HIV-1) VPX (HIV-2) transports cDNA to nucleus in latent
in growing cell--> stops G2 growth phase |
|
|
HIV released by
|
budding or syncytia
|
|
|
4H risk group
|
homosexuals, haitians, hemophiliacs, heroin drug addicts
|
|
|
# people now affected with HIV
|
40 million
|
|
|
2 variant forms of HIV
|
HIV-1 common
HIV-2 west africa, less severe |
|
|
Latent period of HIV
|
long, prodrome like flu
|
|
|
Ryan White
|
9 yo. took away stigma, got from transfusion,
indiana, girl befriended him |
|
|
Genotypes of HIV-1
|
M,N,O
M has 11 subtypes (A-K) |
|
|
clade
|
subtype
|
|
|
HIV-2 has ___ clades
|
6, A-F
|
|
|
AIDS works by (5)
|
reducing CD4 cells
decrease in helpter T cells, delay type hypersensitivity T-cells no activation of CD8 cells increase virion |
|
|
STI of HIV works by
|
enters cell, infects mucosal surface (MALT)
macrophage tropic binds to CD4 marker affects lineage genetic shifts |
|
|
reserviors of HIV
non reservoirs |
macrophage and dendritic cells
peripheral blood and T cells |
|
|
genetic shift of HIV occurs
|
with a change in ENV gene
|
|
|
Acute sx. of HIV
|
2-4 weeks post ex.
burst of virions--> mono/flu symptoms not long duration |
|
|
latent phase of HIV
|
virus decrease
replicate in lymph nodes, macrophages, resting T cells lymphadenopathy (years) 3 months after acute may get rash with aseptic meningitis |
|
|
Late phase of HIV
|
increase viral load
CD4 & 8 decrease no immune responce get secondary infections neurological ramifications |
|
|
AIDS dx by
|
CD4 levels < 200 cells/ microL
|
|
|
neurological ramifications of HIV
|
similar to alzheimers
microglial cells infected macrophages in brain brain produces neurotoxins --> death of neurons cause confusion opportunistic infections in CNS |
|
|
Clinical sx.
|
asx--> AIDS
w/o treatment usually fatal death from CNS involv, cancer (another source), 2nd infection |
|
|
opportunistic infections linked to HIV (7)
|
ARC
Kaposi syndrome pneumocystic pneumonia mycobacterium avium intracellular complex CMV oral candidiasis (thrush) crytococcal meningitis |
|
|
ARC
|
aids related complex
|
|
|
Lab diagnosis important for
|
patient- ID infection, and treatment
ID carriers in latency (transmission follow disease follow treatment |
|
|
Lab dx.
|
serological tests
RT PCR genomic studies Tcell subsets (CD4:cd8 ratio( |
|
|
treatment
|
HAART
|
|
|
HAART
|
highly active anti-retroviral therapy
|
|
|
control of HIV
|
education
safe sex transmission free testing/needles infection control testing donors |
|
|
HTLV
|
many animals affected--> different leukemias and lymphomas
|
|
|
non-human HTLV
|
DIRECT- fast growing
has Vonc (oncogenic gene) virus has growth enhancing proteins |
|
|
human HTLV
|
indirect
slow progression, enhanced by tax protein |
|
|
latency period of HTLV in humans
|
30 years
|
|
|
HTLV associated with leukemias
|
HTLV-1 --> ATLL
HTLV-2 (found in some Hairy cell) HTLV-5 (found in some cutaneous lymphomas) |
|
|
Transmission of HTLV
|
similar to HIV
|
|
|
HTLV infection
|
blood infects CD4 cells --> Delayed type hypersensitivity Tcells--> cutaneous infection and neurons
|
|
|
HTLV can cause ___ but not as bad as HIV
|
immunosuppression
|
|
|
HTLV mainly found in
|
S. Japan, Caribbean, C. africa, African americans in S. E. US
|
|
|
control of HIV
|
education
safe sex transmission free testing/needles infection control testing donors |
|
|
HTLV
|
many animals affected--> different leukemias and lymphomas
|
|
|
non-human HTLV
|
DIRECT- fast growing
has Vonc (oncogenic gene) virus has growth enhancing proteins |
|
|
human HTLV
|
indirect
slow progression, enhanced by tax protein |
|
|
latency period of HTLV in humans
|
30 years
|
|
|
HTLV associated with leukemias
|
HTLV-1 --> ATLL
HTLV-2 (found in some Hairy cell) HTLV-5 (found in some cutaneous lymphomas) |
|
|
Transmission of HTLV
|
similar to HIV
|
|
|
HTLV infection
|
blood infects CD4 cells --> Delayed type hypersensitivity Tcells--> cutaneous infection and neurons
|
|
|
HTLV can cause ___ but not as bad as HIV
|
immunosuppression
|
|
|
HTLV mainly found in
|
S. Japan, Caribbean, C. africa, African americans in S. E. US
|
|
|
clinical sx. of HTLV
|
1:20 --> ATLL
once diagnosed 1 year to live |
|
|
ATLL is
|
neoplasm of CD4 cells, chronic or acute
|
|
|
morphology of ATLL
|
"flower cells" lymphocytes have lobulated nucleus
increase WBC skin lesions (sezary-like) |
|
|
DX of HTLV
|
RT PCR and ELISA
|
|
|
treatment of HTLV
|
AZT with interferon alpha
|
